ArticleThe American journal of pathology1999
Genetic differences in endocrine pancreatic tumor subtypes detected by comparative genomic hybridization.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.
- Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions: the Papanicolaou Society of Cytopathology guidelines for pancreatobiliary cytology.Diagnostic cytopathology · 2014Guideline
- Towards a new classification of gastroenteropancreatic neuroendocrine neoplasms.Nature reviews. Clinical oncology · 2016Review
- Review
- Histologic and Molecular Profile of Pediatric Insulinomas: Evidence of a Paternal Parent-of-Origin Effect.The Journal of clinical endocrinology and metabolism · 2016Article
- Decoding the Molecular and Mutational Ambiguities of Gastroenteropancreatic Neuroendocrine Neoplasm Pathobiology.Cellular and molecular gastroenterology and hepatology · 2015Review
- Novel prognostic markers revealed by a proteomic approach separating benign from malignant insulinomas.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015Article
- Differential expression of genes encoding proteins of the HGF/MET system in insulinomas.Diabetology & metabolic syndrome · 2015Article
- Acinar cell carcinomas of the pancreas: a molecular analysis in a series of 57 cases.Virchows Archiv : an international journal of pathology · 2014Article
- Loss of 11p11 is a frequent and early event in sporadic nonfunctioning pancreatic neuroendocrine neoplasms.Oncology reports · 2014Article
- PI3K-AKT-mTOR-signaling and beyond: the complex network in gastroenteropancreatic neuroendocrine neoplasms.Theranostics · 2014Review
- Utilization of ancillary studies in the cytologic diagnosis of biliary and pancreatic lesions: The Papanicolaou Society of Cytopathology Guidelines.CytoJournal · 2014Article
- Profiling mTOR pathway in neuroendocrine tumors.Targeted oncology · 2012Review
- A case of pancreatic neuroendocrine tumor in a patient with neurofibromatosis-1.World journal of surgical oncology · 2012Article
- Well-differentiated pancreatic neuroendocrine tumors: from genetics to therapy.Nature reviews. Gastroenterology & hepatology · 2012Review
- Molecular cytogenetic characterization in four pediatric pheochromocytomas and paragangliomas.Pathology oncology research : POR · 2011Article
- Localization of sporadic neuroendocrine tumors by gene expression analysis of their metastases.Clinical & experimental metastasis · 2011Article
- The diversity and commonalities of gastroenteropancreatic neuroendocrine tumors.Langenbeck's archives of surgery · 2011Review
- Chromosome 3p alterations in pancreatic endocrine neoplasia.Virchows Archiv : an international journal of pathology · 2011Article
- Insulin secretion and insulin-producing tumors.Expert review of endocrinology & metabolism · 2010Article
- Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular pathogenesis as well as histogenesis of endocrine pancreatic tumors (EPTs) is not well understood, and the clinical behavior of EPTs is difficult to predict using current morphological criteria. Thus, more accurate markers of risk and better understanding of tumor initiation and progression are needed to allow a precise classification of EPTs. We have studied 44 benign and malignant EPTs by comparative genomic hybridization to correlate the overall number of genetic alterations with clinical and histopathological parameters and to identify chromosomal regions which might harbor genes involved in EPT pathogenesis and progression. Aberrations were found in 36 EPTs, and chromosomal losses (mean, 5.3) were slightly more frequent than gains (mean, 4. 6). The most frequent losses involved Y (45% of male EPTs), 6q (39%), 11q (36%), 3p, 3q, 11p (each 30%), 6p (27%), and 10q and Xq (each 25%), whereas most common gains included 7q (43%), 17q (41%), 5q and 14q (each 32%), 7p, 9q, 17p, 20q (each 27%), and 12q and Xp (each 25%). A correlation was found between the total number of genetic changes per tumor and both tumor size and disease stage. In particular, losses of 3p and 6 and gains of 14q and Xq were found to be associated with metastatic disease. Furthermore, characteristic patterns of genetic changes were found in the various EPT subtypes, eg, 6q loss in malignant insulinomas, indicating that these groups might evolve along genetically different pathways. The highlighted genetic aberrations, including the newly found involvement of 6q losses and sex chromosome alterations, should stimulate the further analysis of these chromosomal regions, which may lead to the discovery of novel genes important in the tumorigenesis and evolution of EPTs.
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